This proposal seeks understanding of the capsid assembly process in T4, with a particular interest in the mechanism whereby its genes control capsid length. The main target for study is gene 23 and the protein it encodes, gp23. Mutations that alter capsid development in recognizable ways have been mapped at fourteen sites in gene 23, and mutations as yet unmapped will probably increase that number to twenty or more. The complete nucleotide sequence of gene 23 is now known, and the main thrust of the program will be to determine by sequencing what amino-acid substitutions are responsible for the altered phenotypes of the mutant strains. Two related experiments are also planned. One is to introduce a supernumerary copy of gene 23 into the T4 genome. If such a gene proves to be functional, it can be altered by site-specific directed mutagenesis, and when the normally located gene 23 is deactivated (by unsuppressed amber mutations) the developmental effect of the directed alterations can be analysed. Finally, gene 24 will also be sequenced to assess its homology to gene 23 and the possibility that it may have evolved from a tandem duplication of gene 23.